Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 45, Pages 15030-15033Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3330-10.2010
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Funding
- Wellcome Trust [074618/Z/04]
- MS Society of Great Britain and Northern Ireland
- Department of Health's National Institute for Health Research Biomedical Research Centres
- Higher Education Funding Council for England
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Mitochondrial dysfunction contributes to the pathogenesis of many neurological diseases, including multiple sclerosis (MS), but is not directly measurable in vivo. We modeled N-acetyl-aspartate (NAA), which reflects axonal structural integrity and mitochondrial metabolism, with imaging measures of axonal structural integrity (axial diffusivity and cord cross-sectional area) to extract its mitochondrial metabolic contribution. Lower residual variance in NAA, reflecting reduced mitochondrial metabolism, was associated with greater clinical disability in MS, independent of structural damage.
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